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目的探讨依托咪酯对大鼠脑缺血再灌注损伤的神经保护作用及其机制。方法将120只♂SD大鼠随机均分为假手术组、模型组和依托咪酯高、低剂量组,ip给予各组大鼠相应药物后,采用线栓法制备大脑中动脉栓塞再灌注模型,评价依托咪酯对大鼠脑缺血再灌注的保护作用。参照Bederson评分标准评价大鼠的神经功能损伤,采用TTC染色法观察大鼠的脑梗死体积,采用免疫组化法分析大鼠海马CA1区NAIP、caspase-3及caspase-7蛋白的表达,采用HE染色法观察大鼠脑组织的病理变化。结果与模型组比较,依托咪酯组大鼠的神经功能损伤和脑梗死容积明显减轻,大鼠海马CA1区NAIP蛋白的表达明显增强,caspase-3蛋白的表达明显减少;依托咪酯高、低剂量组间比较无明显差异;各组大鼠海马CA1区caspase-7蛋白的表达无显著差异。结论依托咪酯对大鼠脑缺血再灌注造成的脑损伤具神经细胞保护作用,其机制可能与上调NAIP蛋白的表达、抑制caspase-3蛋白的活化有关。
Objective To investigate the neuroprotective effect of etomidate on cerebral ischemia-reperfusion injury in rats and its mechanism. Methods A total of 120 male SD rats were randomly divided into sham operation group, model group and etomidate high and low dose groups. After administration of the corresponding drugs to rats in each group, the middle cerebral artery occlusion and reperfusion model , Evaluate the protective effect of etomidate on cerebral ischemia-reperfusion in rats. The neurological impairment was evaluated by Bederson score. The infarct volume of rats was observed by TTC staining. The expressions of NAIP, caspase-3 and caspase-7 protein in hippocampal CA1 area were detected by immunohistochemical method. The pathological changes of rat brain were observed by staining. Results Compared with model group, the volume of neurological injury and cerebral infarction in etomidate group was significantly reduced, the expression of NAIP protein in hippocampal CA1 region was significantly increased and the expression of caspase-3 protein was significantly decreased. There was no significant difference between the dose groups; the expression of caspase-7 protein in hippocampal CA1 region of rats in each group had no significant difference. Conclusion Etomidate can protect neurons against brain injury induced by cerebral ischemia-reperfusion in rats. The mechanism may be related to the up-regulation of NAIP protein expression and the inhibition of caspase-3 protein activation.